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Abstract Visual working memory depends on both material-specific brain areas in the ventral visual stream (VVS) that support the maintenance of stimulus representations and on regions in the prefrontal cortex (PFC) that control these representations. How executive control prioritizes working memory contents and whether this affects their representational formats remains an open question, however. Here, we analyzed intracranial EEG (iEEG) recordings in epilepsy patients with electrodes in VVS and PFC who performed a multi-item working memory task involving a retro-cue. We employed Representational Similarity Analysis (RSA) with various Deep Neural Network (DNN) architectures to investigate the representational format of prioritized VWM content. While recurrent DNN representations matched PFC representations in the beta band (15–29 Hz) following the retro-cue, they corresponded to VVS representations in a lower frequency range (3–14 Hz) towards the end of the maintenance period. Our findings highlight the distinct coding schemes and representational formats of prioritized content in VVS and PFC.

Experiencing and remembering objects using the sense of touch is an important aspect of our interactions with our environment, but the cognitive processes of long-term tactile memory for surface textures have not previously been studied. We administered a novel tactile texture memory span task, which required participants to identify new textures among a constantly increasing set of previously experienced stimuli. Performance on that task was compared to a span task employing novel visual objects. We found no correlation between participants' tactile texture span and visual span performance. Additionally, there was no correlation between participants' ability to name textures and their tactile texture span performance. These findings provide some initial evidence for a possible dissociation between long-term memory capacity for stimuli of different sensory modality, and for the mnemonic representation of texture information independent of verbal descriptors.

Abstract Background ADHD is associated with deficits in executive functions. Cognitive training is a promising nonpharmacological intervention for ADHD, however, there is insufficient evidence to guide the selection of training for individuals with ADHD. This pilot study aims to investigate the efficacy of executive function training targeting key executive dysfunctions in ADHD, compared with general executive function training which targets other executive functions. Methods A total of 127 subjects (6–12 years) diagnosed with ADHD were allocated to receive one of two different cognitive trainings. ADHD symptoms and cognitive functions were evaluated using parent-rated scales and CANTAB cognitive assessments. All participants were required to complete 48 training sessions within a two-month period. Results 94 out of 127 children completed the required training and assessments. Both ADHD executive function training group and general executive function training group showed significant improvement in ADHD symptoms on the ADHD Rating Scale and in executive function on the assessment of CANTAB. There was no significant difference in improvements between the two groups. Subgroup analysis suggested that children who had ADHD-RS total scores less than or equal to 28 at baseline showed greater improvement following ADHD executive function training. Conclusions This study indicates that cognitive training can improve ADHD symptoms and executive function, with no difference in efficacy between targeted and generalized cognitive training. In addition, individuals with lower symptom severity may benefit more from training targeting key ADHD executive dysfunctions.

How complex brain functions are mapped onto the human brain is a daunting scientific challenge. Here, the authors use a cognitive neurogenetic approach to identify the structure of executive functions and their underlying neurogenetic basis.

Restudying word lists (e.g., dream, awake, and bed) strengthens true memory of the studied words and reduces false memory for unstudied but semantically related lures (e.g., sleep). Yet, the neural mechanisms involved in this repetition effect on false memory remain unclear. Possible mechanisms involve item-specific and semantic neural representations at encoding, and the memory strength between encoding and retrieval. This study first replicated the behavioral results (Exp. 1) and then investigated various neural mechanisms by using slow event-related functional magnetic resonance imaging (fMRI) and representational similarity analysis (Exp. 2). Behavioral results confirmed that restudy improved true memory and reduced false memory. The fMRI results showed that restudy induced item-specific neural representations at encoding in the left occipital pole, but reduced neural overlap between semantic representations at encoding in the left temporal pole. Individual differences in these two encoding neural mechanisms were correlated with the behavioral measure of false memory, with greater restudy-induced representational changes at encoding (item-specific neural representations and reduced neural overlap between semantic representations) being associated with lower false memory. Moreover, restudy enhanced the memory strength between encoding and retrieval in the visuoparietal cortex but reduced it in the frontal cortex. These findings suggest that dynamic changes in neural representations underlie the repetition effect on false memory, supporting a dual-coding neural framework.

Abstract The aging of the nervous system is a heterogeneous process. It remains a significant challenge to identify relevant markers of pathological and healthy brain aging. A central aspect of aging are decreased sensory acuities, especially because they correlate with the decline in higher cognitive functioning. Sensory and higher cognitive processing relies on information flow between distant brain areas. Aging leads to disintegration of the underlying white matter tracts. While this disintegration is assumed to contribute to higher cognitive decline, data linking structural integrity and sensory function are sparse. The investigation of their interrelation may provide valuable insight into the mechanisms of brain aging. We used a combined behavioral and neuroimaging approach and investigated to what extent changes in microstructural white matter integrity reflect performance declines in tactile pattern recognition with aging. Poor performance in older participants was related to decreased integrity in the anterior corpus callosum. Probabilistic tractography showed that this structure is connected to the prefrontal cortices. Our data point to decreased integrity in the anterior corpus callosum as a marker for advanced brain aging. The correlation between impaired tactile recognition and disintegration in frontal brain networks could provide an explanation why the decrease of sensory function predicts cognitive decline.

New memories can strengthen old memories if the recent and past experience contain elements that are semantically related.

Abstract Mutual influences between anxiety and working memory (WM) have been extensively studied, and their curvilinear relationship resembles the classic Yerkes-Dodson law of arousal and performance. Given the genetic bases of both anxiety and WM, it is likely that the individual differences in the Yerkes-Dodson law of anxiety and WM may have genetic correlates. The current genome wide association study (GWAS) enrolled 1115 healthy subjects to search for genes that are potential moderators of the association between anxiety and WM. Results showed that CPNE3 rs10102229 had the strongest effect, p = 3.38E−6 at SNP level and p = 2.68E−06 at gene level. Anxiety and WM had a significant negative correlation (i.e., more anxious individuals performed worse on the WM tasks) for the TT genotype of rs10102229 (resulting in lower expression of CPNE3), whereas the correlation was positive (i.e., more anxious individuals performed better on the WM tasks) for the CC carriers. The same pattern of results was found at the gene level using gene score analysis. These effects were replicated in an independent sample (N = 330). The current study is the first to report a gene that moderates the relation between anxiety and WM and potentially provides a genetic explanation for the classic Yerkes-Dodson law.

High-dimensionality is ubiquitous in various scientific fields such as imaging genetics, where a deluge of functional and structural data on brain-relevant genetic polymorphisms are investigated. It is crucial to identify which genetic variations are consequential in identifying neurological features of brain connectivity compared to merely random noise. Statistical inference in high-dimensional settings poses multiple challenges involving analytical and computational complexity. A widely implemented strategy in addressing inference goals is penalized inference. In particular, the role of the ridge penalty in high-dimensional prediction and estimation has been actively studied in the past several years. This study focuses on ridge-penalized tests in high-dimensional hypothesis testing problems by proposing and examining a class of methods for choosing the optimal ridge penalty. We present our findings on strategies to improve the statistical power of ridge-penalized tests and what determines the optimal ridge penalty for hypothesis testing. The application of our work to an imaging genetics study and biological research will be presented.

Abstract Background Executive function (EF) is vital to human beings. It has been linked to many genes and family environmental factors in separate studies, but few studies have examined the potential interactions between gene(s) and environmental factor(s). The current study explored the whole genome to identify SNPs, genes, and pathways that interacted with parental warmth (PW) on EF. Results Nine EF tasks were used to measure its three components (common EF, updating, shifting) based on the model proposed by Miyake et al. (2000). We found that rs111605473, LAMP5, SLC4A7, and LRRK1 interacted significantly with PW to affect the updating component of EF, and the GSE43955 pathway interacted significantly with PW to affect the common EF component. Conclusions The current study is the first to identify genes that interacted with PW to affect EF. Further studies are needed to reveal the underlying mechanism.

Brain signal variability has been consistently linked to functional integration; however, whether this coupling is associated with cognitive functions and/or psychiatric diseases has not been clarified. Using multiple multimodality datasets, including resting-state functional magnetic resonance imaging (rsfMRI) data from the Human Connectome Project (HCP: N = 927) and a Beijing sample (N = 416) and cerebral blood flow (CBF) and rsfMRI data from a Hangzhou sample (N = 29), we found that, compared with the existing variability measure (i.e., SDBOLD), the mean-scaled (standardized) fractional standard deviation of the BOLD signal (mfSDBOLD) maintained very high test-retest reliability, showed greater cross-site reliability and was less affected by head motion. We also found strong reproducible couplings between the mfSDBOLD and functional integration measured by the degree centrality (DC), both cross-voxel and cross-subject, which were robust to scanning and preprocessing parameters. Moreover, both mfSDBOLD and DC were correlated with CBF, suggesting a common physiological basis for both measures. Critically, the degree of coupling between mfSDBOLD and long-range DC was positively correlated with individuals’ cognitive total composite scores. Brain regions with greater mismatches between mfSDBOLD and long-range DC were more vulnerable to brain diseases. Our results suggest that BOLD signal variability could serve as a meaningful index of local function that underlies functional integration in the human brain and that a strong coupling between BOLD signal variability and functional integration may serve as a hallmark of balanced brain networks that are associated with optimal brain functions.

Although human memories seem unique to each individual, they are shared to a great extent across individuals. Previous studies have examined, separately, subject-specific and cross-subject shared representations during memory encoding and retrieval, but how shared memories are formed from individually encoded representations is not clearly understood. Using a unique fMRI design involving memory encoding and retrieval, and representational similarity analysis to link representations from different individuals, brain regions, and processing stages, the current study revealed that distributed brain regions showed both subject-specific and shared neural representations during both memory encoding and retrieval. Furthermore, different brain regions showed stage-specific representational strength, with the visual cortex showing greater unique and shared representations during encoding, whereas the left angular gyrus showing greater unique and shared representations during retrieval. The neural representations during encoding were transformed during retrieval, as shown by smaller cross-subject encoding-retrieval similarity (ERS) than cross-subject similarity either during encoding or during retrieval. This cross-subject and cross-stage similarity was found both within and across regions, with strong pattern similarity between the encoded representation in VVC and the retrieved representation in the angular gyrus. Simulation analysis further suggested that these patterns could be achieved by incorporating stage-specific representational strength, and cross-region reinstatement from encoding to retrieval, but not by a common transformation from encoding to retrieval across subjects. Together, our results shed light on how memory representations are encoded and transformed to maintain individual characteristics and at the same time to create shared representations to facilitate interpersonal communication.

Updating old memories with new, more current information is critical for human survival, yet the neural mechanisms for memory updating in general and the effect of retrieval practice in particular are poorly understood. Using a three-day A-B/A-C memory updating paradigm, we found that compared to restudy, retrieval practice could strengthen new A-C memories and reduce old A-B memory intrusion, but did not suppress A-B memories. Neural activation pattern analysis revealed that compared to restudy, retrieval practice led to stronger target representation in the medial prefrontal cortex (MPFC) during the final test. Critically, it was only under the retrieval practice condition that the MPFC showed strong and comparable competitor evidence for both correct and incorrect trials during final test, and that the MPFC target representation during updating was predictive of subsequent memory. These results suggest that retrieval practice is able to facilitate memory updating by strongly engaging MPFC mechanisms in memory integration, differentiation and consolidation.

One of the pivotal challenges of aging is to maintain independence in the activities of daily life. In order to adapt to changes in the environment, it is crucial to continuously process and accurately combine simultaneous input from different sensory systems, i.e., crossmodal or multisensory integration. With aging, performance decreases in multiple domains, affecting bottom-up sensory processing as well as top-down control. However, whether this decline leads to impairments in crossmodal interactions remains an unresolved question. While some researchers propose that crossmodal interactions degrade with age, others suggest that they are conserved or even gain compensatory importance. To address this question, we compared the behavioral performance of older and young participants in a well-established crossmodal matching task, requiring the evaluation of congruency in simultaneously presented visual and tactile patterns. Older participants performed significantly worse than young controls in the crossmodal task when being stimulated at their individual unimodal visual and tactile perception thresholds. Performance increased with adjustment of stimulus intensities. This improvement was driven by better detection of congruent stimulus pairs, while the detection of incongruent pairs was not significantly enhanced. These results indicate that age-related impairments lead to poor performance in complex crossmodal scenarios and demanding cognitive tasks. Crossmodal congruency effects attenuate the difficulties of older adults in visuotactile pattern matching and might be an important factor to drive the benefits of older adults demonstrated in various crossmodal integration scenarios. Congruency effects might, therefore, be used to develop strategies for cognitive training and neurological rehabilitation.

More than 100 risk loci for schizophrenia have been identified by genome-wide association studies. Here, the authors apply an integrative genomic approach to prioritize risk genes and validate GLT8D1 and CSNK2B as candidate causal genes by in vitro studies in neural stem cells.

Risk-taking is purported to be central to addictive behaviors. However, for Internet gaming disorder (IGD), a condition conceptualized as a behavioral addiction, the neural processes underlying impaired decision-making (risk evaluation and outcome processing) related to gains and losses have not been systematically investigated. Forty-one males with IGD and 27 healthy comparison (HC) male participants were recruited, and the cups task was used to identify neural processes associated with gain- and loss-related risk- and outcome-processing in IGD. During risk evaluation, the IGD group, compared to the HC participants, showed weaker modulation for experienced risk within the bilateral dorsolateral prefrontal cortex (DLPFC) (t = −4.07; t = −3.94; PFWE

It has been shown that reward motivation can facilitate proactive control, a cognitive control mode that is characterized of prior preparation and sustained holding of the goal-relevant information in working memory. However, it remains to be established the neural networks that may be involved in this promotion effect. In this study, participants underwent the AX-Continuous Performance Task (AX-CPT) that measures relative proactive control during functional magnetic resonance imaging (fMRI) scanning. We employed independent component analysis to decompose multiple brain networks and identified the task related network. Results showed that the salience network (SN) was engaged in the AX-CPT protocol. Importantly, our data demonstrated that reward modulated the association between task engagement of SN and proactive control, whereby the positive correlation was particularly observed in the reward condition. Moreover, reward modulated task engagement of the SN in a proactive manner, which may contribute to the behavioral proactive performance. Overall, our data suggest the involvement of SN in the reward facilitation effect of proactive control.

Previous studies have revealed that greater neural pattern similarity across repetitions is associated with better subsequent memory. In this study, we used an artificial language training paradigm and representational similarity analysis to examine whether neural pattern similarity across repetitions before training was associated with post-training behavioral performance. Twenty-four native Chinese speakers were trained to learn a logographic artificial language for 12 days and behavioral performance was recorded using the word naming and picture naming tasks. Participants were scanned while performing a passive viewing task before training, after 4-day training and after 12-day training. Results showed that pattern similarity in the left pars opercularis (PO) and fusiform gyrus (FG) before training was negatively associated with reaction time (RT) in both word naming and picture naming tasks after training. These results suggest that neural pattern similarity is an effective neurofunctional predictor of novel word learning in addition to word memory.

Transcranial direct current stimulation (tDCS) is a widely-used tool to induce neuroplasticity and modulate cortical function by applying weak direct current over the scalp. In this review, we first introduce the underlying mechanism of action, the brief history from discovery to clinical scientific research, electrode positioning and montages, and parameter setup of tDCS. Then, we review tDCS application in clinical samples including people with drug addiction, major depression disorder, Alzheimer's disease, as well as in children. This review covers the typical characteristics and the underlying neural mechanisms of tDCS treatment in such studies. This is followed by a discussion of safety, especially when the current intensity is increased or the stimulation duration is prolonged. Given such concerns, we provide detailed suggestions regarding safety procedures for tDCS operation. Lastly, future research directions are discussed. They include foci on the development of multi-tech combination with tDCS such as with TMS and fMRI; long-term behavioral and morphological changes; possible applications in other research domains, and more animal research to deepen the understanding of the biological and physiological mechanisms of tDCS stimulation.

Catechol-O-methyltransferase (COMT) and brain-derived neurotrophic factor (BDNF) genes have been found to interactively influence working memory (WM) as well as brain activation during WM tasks. However, whether the two genes have interactive effects on resting-state activities of the brain and whether these spontaneous activations correlate with WM are still unknown. This study included behavioral data from WM tasks and genetic data (COMT rs4680 and BDNF Val66Met) from 417 healthy Chinese adults and resting-state fMRI data from 298 of them. Significant interactive effects of BDNF and COMT were found for WM performance as well as for resting-state regional homogeneity (ReHo) in WM-related brain areas, including the left medial frontal gyrus (lMeFG), left superior frontal gyrus (lSFG), right superior and medial frontal gyrus (rSMFG), right medial orbitofrontal gyrus (rMOFG), right middle frontal gyrus (rMFG), precuneus, bilateral superior temporal gyrus, left superior occipital gyrus, right middle occipital gyrus and right inferior parietal lobule. Simple effects analyses showed that compared to other genotypes, subjects with COMT-VV/BDNF-VV had higher WM and lower ReHo in all five frontal brain areas. The results supported the hypothesis that COMT and BDNF polymorphisms influence WM performance and spontaneous brain activity (i.e., ReHo).

Previous correlational imaging studies have implicated the dorsolateral prefrontal cortex (DLPFC) in decision making. Using High-Definition Transcranial Direct Current Stimulation (HD-tDCS), the present study directly investigated the causal role of the DLPFC in performing the Iowa Gambling Task (IGT) and the Inter-Temporal Choice (ITC) task. Three experiments were conducted: Exp. 1 (N = 41) to study the left DLPFC, Exp. 2 (N = 49) to study the right DLPFC, and Exp. 3 (N = 20, a subset of those in Exp. 1) to switch the experimental and control conditions. All participants were healthy male college students. For Exps. 1 and 2, participants were randomly assigned to either the HD- tDCS or the sham stimulation condition. For Exp. 3, participants were assigned to the condition they were not in during Exp. 1. Results showed that HD-tDCS over the left DLPFC increased IGT score, decreased the recency parameter in IGT, and lowered delay discounting rate (k) in the ITC task. We discussed the potential roles of impulse control and time perception in mediating the effect of tDCS stimulation of left DLPFC on decision making. Our results have clinical implications for the treatment of disorders involving poor decision-making, such as addictions.

The striatum is an important subcortical structure with extensive connections to other regions of the brain. These connections are believed to play important roles in behaviors such as reward-related processes and impulse control, which show significant sex differences. However, little is known about sex differences in the striatum-projected fiber connectivity. The current study examined sex differences between 50 Chinese males and 79 Chinese females in their fiber connections between the striatum and nine selected cortical and subcortical regions. Despite overall similarities, males showed stronger fiber connections between the left caudate and rostral cingulate cortex, between the right putamen and the lateral orbitofrontal cortex, between the bilateral putamen and the ventro-lateral prefrontal cortex, and between the right caudate and the ventro-lateral prefrontal cortex, whereas females showed stronger fiber connections between the right putamen and the dorsolateral prefrontal cortex, between bilateral caudate and hippocampus, and between the left putamen and hippocampus. These findings help us to understand sex differences in the striatum-projected fiber connections and their implications for sex differences in behaviors.

Cooperativeness is an essential behavioral trait evolved to facilitate group living. Social and cognitive mechanisms involved in cooperation (e.g., motivation, reward encoding, action evaluation, and executive functions) are sub-served by the striatal-projected circuits, whose physical existence has been confirmed by animal studies, human postmortem studies, and in vivo human brain studies. The current study investigated the associations between Cooperativeness and fiber connectivities from the striatum to nine subcortical and cortical regions, including the amygdala, hippocampus, medial orbitofrontal cortex, lateral orbitofrontal cortex, ventrolateral prefrontal cortex, dorsolateral prefrontal cortex, posterior cingulate cortex/retrosplenial cortex, dorsal cingulate cortex, and rostral cingulate cortex. Results showed that Cooperativeness was negatively correlated with fiber connectivity for the cognitive control system (from the dorsal caudate to the rostral cingulate cortex and ventrolateral prefrontal cortex), but not with fiber connectivity for the social cognitive system (e.g., connectivity with the medial prefrontal cortex and amygdala). These results partially supported Declerck et al.'s (2013) cognitive neural model of the role of cognitive control and social cognition in cooperation.

In the original version of this Article, the affiliation details for Qiushuo Shen incorrectly omitted ‘Kunming College of Life Science, University of Chinese Academy of Sciences, Kunming, 650204, China’. This has now been corrected in both the PDF and HTML versions of the Article.

Sensory processing sensitivity (SPS) is an intrinsic personality trait whose genetic and neural bases have recently been studied. The current study used a neural mediation model to explore whether resting-state brain functions mediated the effects of dopamine-related genes on SPS. 298 healthy Chinese college students (96 males, mean age = 20.42 years, SD = 0.89) were scanned with magnetic resonance imaging during resting state, genotyped for 98 loci within the dopamine system, and administered the Highly Sensitive Person Scale. We extracted a "gene score" that summarized the genetic variations representing the 10 loci that were significantly linked to SPS, and then used path analysis to search for brain regions whose resting-state data would help explain the gene-behavior association. Mediation analysis revealed that temporal homogeneity of regional spontaneous activity (ReHo) in the precuneus actually suppressed the effect of dopamine-related genes on SPS. The path model explained 16% of the variance of SPS. This study represents the first attempt at using a multi-gene voxel-based neural mediation model to explore the complex relations among genes, brain, and personality.

Although behavioral and neuropsychological studies have suggested two distinct routes of phonological access, their neural substrates have not been clearly elucidated. Here, we designed an artificial language (based on Korean Hangul) that can be read either through addressed (i.e., whole word mapping) or assembled (i.e., grapheme-to-phoneme mapping) phonology. Two matched groups of native English-speaking participants were trained in one of the two conditions, one hour per day for eight days. Behavioral results showed that both groups correctly named more than 90% of the trained words after training. At the neural level, we found a clear dissociation of the neural pathways for addressed and assembled phonologies: There was greater involvement of the anterior cingulate cortex, posterior cingulate cortex, right orbital frontal cortex, angular gyrus and middle temporal gyrus for addressed phonology, but stronger activation in the left precentral gyrus/inferior frontal gyrus and supramarginal gyrus for assembled phonology. Furthermore, we found evidence supporting the strategy-shift hypothesis, which postulates that, with practice, reading strategy shifts from assembled to addressed phonology. Specifically, compared to untrained words, trained words in the assembled phonology group showed stronger activation in the addressed phonology network and less activation in the assembled phonology network. Our results provide clear brain-imaging evidence for the dual-route models of reading.

Many real-life decisions in complex and changing environments are guided by the decision maker's beliefs, such as her perceived control over decision outcomes (i.e., agency), leading to phenomena like the "illusion of control". However, the neural mechanisms underlying the "agency" effect on belief-based decisions are not well understood. Using functional imaging and a card guessing game, we revealed that the agency manipulation (i.e., either asking the subjects (SG) or the computer (CG) to guess the location of the winning card) not only affected the size of subjects' bets, but also their "world model" regarding the outcome dependency. Functional imaging results revealed that the decision-related activation in the lateral and medial prefrontal cortex (PFC) was significantly modulated by agency and previous outcome. Specifically, these PFC regions showed stronger activation when subjects made decisions after losses than after wins under the CG condition, but the pattern was reversed under the SG condition. Furthermore, subjects with high external attribution of negative events were more affected by agency at the behavioral and neural levels. These results suggest that the prefrontal decision-making system can be modulated by abstract beliefs, and are thus vulnerable to factors such as false agency and attribution.

Impairments in flexible goal-directed decisions, often examined by reversal learning, are associated with behavioral abnormalities characterized by impulsiveness and disinhibition. Although the lateral orbital frontal cortex (OFC) has been consistently implicated in reversal learning, it is still unclear whether this region is involved in negative feedback processing, behavioral control, or both, and whether reward and punishment might have different effects on lateral OFC involvement. Using a relatively large sample (N = 47), and a categorical learning task with either monetary reward or moderate electric shock as feedback, we found overlapping activations in the right lateral OFC (and adjacent insula) for reward and punishment reversal learning when comparing correct reversal trials with correct acquisition trials, whereas we found overlapping activations in the right dorsolateral prefrontal cortex (DLPFC) when negative feedback signaled contingency change. The right lateral OFC and DLPFC also showed greater sensitivity to punishment than did their left homologues, indicating an asymmetry in how punishment is processed. We propose that the right lateral OFC and anterior insula are important for transforming affective feedback to behavioral adjustment, whereas the right DLPFC is involved in higher level attention control. These results provide insight into the neural mechanisms of reversal learning and behavioral flexibility, which can be leveraged to understand risky behaviors among vulnerable populations.

Humans demonstrate an inherent bias towards making maladaptive decisions, as shown by a phenomenon known as the gambler's fallacy (GF). The GF has been traditionally considered as a heuristic bias supported by the fast and automatic intuition system, which can be overcome by the reasoning system. The present study examined an intriguing hypothesis, based on emerging evidence from neuroscience research, that the GF might be attributed to a weak affective but strong cognitive decision making mechanism. With data from a large sample of college students, we found that individuals' use of the GF strategy was positively correlated with their general intelligence and executive function, such as working memory and conflict resolution, but negatively correlated with their affective decision making capacities, as measured by the Iowa Gambling Task. Our result provides a novel insight into the mechanisms underlying the GF, which highlights the significant role of affective mechanisms in adaptive decision-making.

BACKGROUND: Recent molecular genetics studies showed significant associations between dopamine-related genes (including genes for dopamine receptors, transporters, and degradation) and working memory, but little is known about the role of genes for dopamine modulation, such as those related to neurotensin (NT), in working memory. A recent animal study has suggested that NT antagonist administration impaired working memory in a learning task. The current study examined associations between NT genes and working memory among humans. METHODS: Four hundred and sixty healthy undergraduate students were assessed with a 2-back working memory paradigm. 5 SNPs in the NTSR1 gene were genotyped. 5 ANOVA tests were conducted to examine whether and how working memory differed by NTSR1 genotype, with each SNP variant as the independent variable and the average accuracy on the working memory task as the dependent variable. RESULTS: ANOVA results suggested that two SNPs in the NTSR1 gene (rs4334545 and rs6090453) were significantly associated with working memory. These results survived corrections for multiple comparisons. CONCLUSIONS: Our results demonstrated that NTSR1 SNP polymorphisms were significantly associated with variance in working memory performance among healthy adults. This result extended previous rodent studies showing that the NT deficiency impairs the working memory function. Future research should replicate our findings and extend to an examination of other dopamine modulators.

The left midfusiform and adjacent regions have been implicated in processing and memorizing familiar words, yet its role in memorizing novel characters has not been well understood.Using functional MRI, the present study examined the hypothesis that the left midfusiform is also involved in memorizing novel characters and spaced learning could enhance the memory by enhancing the left midfusiform activity during learning. Nineteen native Chinese readers were scanned while memorizing the visual form of 120 Korean characters that were novel to the subjects. Each character was repeated four times during learning. Repetition suppression was manipulated by using two different repetition schedules: massed learning and spaced learning, pseudo-randomly mixed within the same scanning session. Under the massed learning condition, the four repetitions were consecutive (with a jittered inter-repetition interval to improve the design efficiency). Under the spaced learning condition, the four repetitions were interleaved with a minimal inter-repetition lag of 6 stimuli. Spaced learning significantly improved participants' performance during the recognition memory test administered one hour after the scan. Stronger left midfusiform and inferior temporal gyrus activities during learning (summed across four repetitions) were associated with better memory of the characters, based on both within- and cross-subjects analyses. Compared to massed learning, spaced learning significantly reduced neural repetition suppression and increased the overall activities in these regions, which were associated with better memory for novel characters.These results demonstrated a strong link between cortical activity in the left midfusiform and memory for novel characters, and thus challenge the visual word form area (VWFA) hypothesis. Our results also shed light on the neural mechanisms of the spacing effect in memorizing novel characters.